Fig. 5: Increased energy metabolism and promotion of mineralization in Dnmt1-deficient mice.
From: Dnmt1 determines bone length by regulating energy metabolism of growth plate chondrocytes
A Glutamine uptake by Dnmt1flox (n = 3) and Dnmt1ΔPrx1 (n = 3) chondrocytes. B Left panel: Oxygen consumption rate (OCR) assessed after addition of oligomycin, carbonyl cyanide 4- (trifluoromethoxy) phenylhydrazone (FCCP), and antimycin A/rotenone (AA/ROT) at the indicated times. Right panel: Basal respiration, ATP production and maximal respiration measured for Dnmt1flox (n = 3) and Dnmt1ΔPrx1 (n = 3) chondrocytes. C Relative quantification of energy metabolites by metabolome analysis of Dnmt1flox (n = 7) and Dnmt1ΔPrx1 (n = 9) chondrocytes. D Calcification activity in primary cultured chondrocytes in the presence or absence of glucose, glutamine, and pyruvate as evaluated by Alizarin Red staining of Dnmt1flox (n = 5) and Dnmt1ΔPrx1 (n = 5) chondrocytes. E Calcification activity in Dnmt1flox and Dnmt1ΔPrx1 micromass cultured chondrocytes in the presence of energy metabolism inhibitors (CB839: Glutaminase inhibitor (n = 4), Oligomycin: ATP synthesis inhibitor (n = 4)) as evaluated by Alizarin Red staining. F µCT images of Dnmt1ΔPrx1 tibia treated with DMSO or CB839. The yellow dashed line indicates the area around the primary trabecular bone analyzed by µCT. Representative data from at least three individual mice are shown. Quantitative analysis of (G) trabecular and (H) cortical bone parameters by μCT in DMSO (n = 6) or CB839 (n = 6) treatment. All data are mean ± s.d. Significance of mean differences was assessed using unpaired t-tests or Tukey’s post hoc tests with two-tailed P values. Source data are provided as a Source Data file.
